Background/purpose: This study was conducted retrospectively to examine whether laparoscopic splenectomy is an effective procedure for patients with splenomegaly due to portal hypertension in comparison to patients with a normal-sized spleen.
Methods: From September 1994 to May 2005, we performed laparoscopic splenectomy in 50 patients at Wakayama Medical University Hospital, Japan. Of these, 17 patients with splenomegaly due to portal hypertension and 17 patients with idiopathic thrombocytopenic purpura (ITP) with normal-size spleen were enrolled in this study, in which we compared the surgical outcome between patients with splenomegaly due to portal hypertension and those without splenomegaly (ITP group).
Results: The mean operative time (splenomegaly due to portal hypertension vs ITP; 171 vs 165 min; P = 0.7433) and estimated blood loss (248 vs 258 ml; P = 0.5396) were similar in the two groups. There were two patients with complications (11.8%) in the patients with splenomegaly due to portal hypertension and five patients with complications (29.4%) in those with ITP. All patients with splenomegaly due to portal hypertension showed appropriate increases in the platelet count following surgery. No perioperative mortality occurred.
Conclusions: We concluded that laparoscopic splenectomy was an effective procedure for splenomegaly due to portal hypertension, with findings being similar to those observed in patients with a normal-sized spleen (such as patients with ITP).
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http://dx.doi.org/10.1007/s00534-007-1232-7 | DOI Listing |
Clin J Gastroenterol
December 2024
Department of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, 514-8507, Japan.
Front Immunol
December 2024
National and Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Introduction: Portal hypertension combined with hypersplenism (PHcH) is the main cause of hypocytosis and esophagogastric variceal hemorrhage in patients with liver cirrhosis. Activated macrophages that destroy excess blood cells are the main cause of hypersplenism, but the activating pathway is not very clear. This study aims to investigate the activation types of splenic macrophages and their activation mechanisms, to provide experimental evidence for the biological treatment of splenomegaly, and to find a strategy to improve liver fibrosis and inflammation by intervening in splenic immune cells.
View Article and Find Full Text PDFHepatol Res
November 2024
Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.
Partial splenic embolization (PSE) has developed as an alternative to surgical splenectomy, mainly to improve hypersplenism and esophagogastric varices in cirrhotic patients. We proposed the novel concept that splenic infarction volume, rather than the splenic infarction ratio, is essential for patients receiving PSE. A splenic infarction volume between 388 and 540 mL is suitable for a sufficient increase in platelet count and less severe PSE-related complications.
View Article and Find Full Text PDFRadiol Case Rep
January 2025
Faculty of Diagnostic Radiology, University of Calgary, Calgary, Alberta, Canada.
A 51-year-old man, with a history of cirrhotic portal hypertension and recurrent transjugular intrahepatic portosystemic shunt (TIPS) stenoses, presented with an acute gastro-esophageal variceal hemorrhage in the setting of an acute and massive thrombotic TIPS shunt occlusion. The clinical presentation was complicated by patient's severe, chronic thrombocytopenia which had precluded empiric anticoagulation previously for recurrent TIPS dysfunction. Following endoscopic treatment of the variceal bleeding, the CAT 12 Indigo aspiration system (Penumbra) was used to remove a large burden of thrombus from the TIPS, allowing successful re-stenting and restoration of blood flow through the TIPS.
View Article and Find Full Text PDFSurg Case Rep
November 2024
Department of Diagnostic Pathology, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
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